 Faculty Profiles
The Schnell lab is investigating cell physiology systems comprising many interacting components, where modeling and theory may aid in the identification of the key mechanisms underlying the behavior of the system as a whole. We are currently focusing in three areas:
(1) Molecular mechanisms of b-cell dysfunction. Pancreatic β-cell failure is increasingly recognized as central to the progression of diabetes mellitus. Different causes are implicated in the onset of β-cell stress, dysfunction or dead. Failure in modulating the capacity and quality of the endoplasmic reticulum protein-folding machinery leads to β-cell dead. The quality control of protein-folding is regulated by several signaling pathways, which are collectively termed the unfolded protein response. In the β-cells proinsulin represents up to 50% of the total protein synthesis, and the rate of glucose-stimulated proinsulin translation is approximately 1 million molecules per minute per cell. We are investigating how the high burden imposed by the insulin biosynthesis on the unfolded protein response can be a leading cause of certain diabetes phenotypes.
(2) The role of macromolecular crowding in cell physiology. Nowadays there is no doubt that living cells have high macromolecular content. Does this mean that macromolecular crowding is essential to life? As far as we know, all modern cells have a high macromolecular content. In fact, it is now recognize that cells must have a mechanism for the synthesis and regulation of crowding agents. This system seems to be energetically expensive. If evolution has selected cells maintaining a high macromolecular content, crowding must be important for the cell. We are investigating the role that crowding is playing in the cell physiology and reactions occurring inside cells.
(3) Mechanism of cellular guidance in cell migration. There are certain stem cell-like populations which are highly invasive and contribute to embryonic development and tumor formation. The physiological mechanisms driving the migration of these cells are not fully understood. We are investigating how migratory cells interpret signals from the microenvironments and other cells to reach their precise targets.
S. Schnell and C. Mendoza (1997). A closed-form solution for time-dependent enzyme kinetic. Journal of theoretical Biology 187, 207-212.
S. Schnell and P. K. Maini (2000). Clock and induction model for somitogenesis. Developmental Dynamics 217, 415-420.
S. Schnell and P. K. Maini (2000). Enzyme kinetics at high enzyme concentration. Bulletin of Mathematical Biology 62, 483-499.
S. Schnell and P. K. Maini (2003). A century of enzyme kinetics: Reliability of the KM and vmax estimates. Comments on Theoretical Biology 8, 169-187
E. J. Crampin, S. Schnell and P. McSharry (2004). Mathematical and computational techniques to deduce complex biochemical reaction mechanisms. Progress in Biophysics and Molecular Biology 86, 77-112.
S. Schnell and T. E. Turner (2004). Reaction kinetics in intracellular environments with macromolecular crowding: simulations and rate laws. Progress in Biophysics and Molecular Biology 85, 235-260.
T. E. Turner, S. Schnell and K. Burrage (2004). Stochastic approaches for modelling in vivo reactions. Computational Biology and Chemistry 28, 165-178.
B. Ribba, T. Collin and S. Schnell (2006). A multiscale mathematical model of cancer, and its use in analyzing irradiation therapies. Theoretical Biology and Medical Modelling 3, 7.
R. Grima and S. Schnell (2006). A systematic investigation of the rate laws valid in intracellular environments. Biophysical Chemistry 124, 1-10.
J. Srividhya, E. J. Crampin, P. E. McSharry and S. Schnell (2007). Reconstructing biochemical pathways from time course data. Proteomics 7, 828-838.
R. Grima and S. Schnell (2007). Can tissue surface tension drive somite formation? Developmental Biology 307, 248-257.
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